The specific aim of this study is to confirm the efficacy of combination androstane therapy with etiocholanolone (3a) and androgens in patients with aplatic anemia refractory to immunosuppressive therapy. The study will enroll a total of 25 patients with aplastic anemia, who have failed immunosuppressive therapy. 3a-etiocholanolone mixed with prednisone and testosterone will be administered intramuscularly for at least 3 months and response evaluated. If at the end of the first 12 weeks, the marrow scan indicates recovery in the absence of a change of blood counts, therapy will be extended another 12 weeks. Two patients (1 male, 1 female) were enrolled on the study. Both patients completed the study. Patient #1 had a pancytopenia and a hypoplastic bone marrow at onset of study and on a biopsy two years prior to the study. Cytogenetics study prior to the therapy was reported as an inadequate study. Patient continued to be RBC & platelet transfusion dependent through the study period except for slight decrease in RBC transfusions. Patient was on Neupogen until about 1 month prior to enrollment into the study. After study entry the patients AGC dropped to <200/fl because of effect of Neupogen which he was on before wore off. Neupogen was restored with an resultant increase in the WBC of up to 22,000. Notably, on RBC histograms a macrocytic population of RBC became apparent while on therapy with ET/Nandrolone decanoate and Neupogen. A repeat marrow scan showed extension of marrow activity following therapy. For these reasons, per protocol, ET/Nandrolone were continued past Day 84. On blood tests of Day 112 of study, an increase in liver enzymes was noted and study drugs (but not Neupogen) was stopped. Over the next several weeks the liver enzymes returned to the prestudy levels. Despite the production of a macrocytic subpopulation of RBCs the patient's pancytopenia did not respond to therapy. A repeat bone marrow and cytogenetics at Day 90 of the study showed a cellular bone marrow with dysplastic features and presence of an abnormal cytogenetics). The patient had pancytopenia 2o a hypoplastic MDS which concerted to a cellular form either spontaneously or likely 2o Neupogen. ET/Nandrolone therapy was ineffective in this patient with myelodysplasia, even though a macrocytic population of RBC was induced by the therapy. Patient #2 was a 50 year old white female with a biopsy proven aplastic anemia. The chromosomal analysis at enrollment revealed a normal 46XX pattern. A dose of 28-32 mg per dose of etiocholanolone, 3X/wk was administered until day 42 at which time a large hematoma was noted at site of a Nandrolone decanoate injection which had been administered incorrectly by the spouse. Because of this, therapy was irregular as sites to inject ET & Nandrolone became less available. The hematoma resorbed over the next 5-6 weeks. Patient's transfusion dependence on RBC's continued. Platelets were given in case of bleeding only as patient was refractory to platelet transfusions. On November 28, 1997 (Day 72) the patient was admitted to the hospital with a febrile neutropenia and treated with broad spectrum antibiotics. She recovered and was discharged on December 6, 1997 (Day 80). She was readmitted the same day with bleeding per rectum and had a new onset neutropenic fever two days later. End of study evaluation on Day 84 revealed a persistence of severe aplastic anemia. The patient was expired on Day 89 with diffuse pulmonary infiltrates and developed multiple organ system failure terminally. Life support was discontinued, as per patients living will and in keeping with the family's wishes. The patient failed therapy for the aplastic anemia with ET/Prednisolone/ Nandrolone. Notably, the drug administration was sub-optimal due to the hematoma. Pharmacokinetic studies were completed on both patients on Day 1 and Day 28.